Pedunculopontine tegmental (PPT) GABAergic system plays a crucial role in the regulation of rapid eye movement (REM) sleep. We recently reported that the activation of PPT GABA-B receptors suppressed REM sleep by inhibiting REM-on cells. One of the important mechanisms for GABA-B receptor-activation-mediated physiological action is the inhibition of intracellular cAMP-dependent PKA (cAMP-PKA) signaling pathway. Accordingly, we hypothesized that the PPT GABA-B receptor activation-mediated REM sleep suppression effect could be mediated via inhibition of cAMP-PKA activation. To test this hypothesis, a GABA-B receptor selective agonist, Baclofen hydrochloride (Baclofen), cAMP-PKA activator, Sp-Adenosine 3',5'-cyclic monophosphothioate triethylamine (SpCAMPS), and vehicle control were microinjected into the PPT in selected combinations to determine effects on sleep-waking states of chronically instrumented, freely moving rats. Microinjection of SpCAMPS (1.5 nmol) induced REM sleep within a short latency (12.1 ± 3.6 minutes) compared to vehicle control microinjection (60.0 ± 6.5 minutes). On the contrary, microinjection of Baclofen (1.5 nmol) suppressed REM sleep by delaying its appearance for about 183 minutes; however, the suppression of REM sleep by Baclofen was prevented by a subsequent microinjection of SpCAMPS. These results provide evidence that the activation of cAMP-PKA within the PPT can successfully block GABA-B receptor activation mediated REM sleep suppression effect. These findings suggest that the PPT GABA-B receptor activation-mediated REM sleep regulating mechanism involves inactivation of cAMP-PKA signaling in the freely moving rat.